Activation of human oncogenes: The long terminal repeat (LTR) of the Abelson murine leukemia virus (A-MuLV), in combination with other 5 feet terminal sequences of various lengths, were covalently linked to two human cellular oncogenes--human c-sis, and human c-bas/has. In contrast to human c-sis, which could not be activated by the LTR promotor, the human bas/has fragment was activated into a transforming efficiency of 10 ffu per Mug DNA by upstream linkage to three out of the four LTR vectors. On the other hand, neither the 5 feet LTR nor the 3 feet LTR, when linked to the c-bas/has in the downstream position, conferred any transforming activation. Experiments are being performed to clarify the factors responsible for activation of the normal human bas/has oncogene. Identification of coding sequences responsible for transformation activity: A series of recombinant plasmids containing deletions in the various exons of the transforming human c-bas/has gene are now being constructed and checked for transformation efficiency on NIH-3T3 cells. This is being performed with the aim of localizing the regions responsible for accurate expression of p21. Retroviruses as cloning vectors for mammalian oncogenes: A retrovirus vector was constructed by inserting the activated human c-bas into an A-MuLV construct. Experiments are being performed to rescue the oncogene-containing viral particles by superinfection with replication-competent retrovirus.